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Introduction:The activated clotting time (ACT) is a useful marker of unfractionated heparin (UFH) activity during cardiopulmonary bypass (CPB) or cardiac catheterization. Emicizumab, recently approved for bleeding prevention in haemophilia A patients, acts like FVIII but does not need prior activation; it therefore shortens coagulation times in assays using intrinsic pathway activators and so is expected to shorten the ACT.Aim: To evaluated emicizumab's impact on heparin-induced ACT (Hemochron®) prolongation. Methods:We measured the high-range (HR) ACT in citrated blood samples from healthy donors (HDs) (n = 9), CPB patients (n = 3) and emicizumab-treated patients (n = 5) after spiking with UFH and/or emicizumab. The low range (LR) ACT was also measured in spiked-samples from HDs and emicizumab-treated patients. Results:In HDs, the median [interquartile range] baseline HR-ACTs were similar with and without emicizumab (129 [123-138] and 136 s for 50 µg/ml, respectively); whatever the concentration of emicizumab (10 to 50 µg/ml), increasing the UFH concentration (1-5 UI/ml) prolonged the HR-ACT. In blood from patients undergoing CPB, the HR-ACT prolongation observed during this procedure was not masked by emicizumab at any concentration. Likewise, the addition of increasing concentrations of UFH to blood from emicizumab-treated patients induced a concentrationdependent prolongation of HR-ACT. Baseline LR-ACT were prolonged in emicizumabtreated patients but as for HR-ACT, emicizumab does not prevent heparin-induced prolongation of LR-ACT. Conclusion:Emicizumab does not interfere with UFH-induced ACT prolongation. The hemochron® ACT can be used to monitor UFH in patients receiving emicizumab during CPB or cardiac catheterization.